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Smart, Injury-Triggered Therapy for Ocular Trauma

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Annual rept. 15 Sep 2014-14 Sep 2015

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Traumatic eye injury TEI is one of the leading causes of monocular blindness in military personnel and young males worldwide. This profound and frequently irreversible posttraumatic loss of vision has a poor prognosis due to retinal cell death, scar formation, and lack of functional regeneration. Proliferative vitreoretinopathy PVR, a form of intraocular fibrosis, is often the primary reason for the loss of vision after ocular trauma, and frequently occurs after blunt trauma and open globe injuries caused by penetration, rupture, perforation, and presence of intraocular foreign bodies as well as after retinal re-attachment surgery. We genetically engineered protease activity sensor PAS as chimeric transmembrane protein that can respond to increase in metalloproteinase activity by sheddingreleasing tagged-ectodomains in the vicinity of affected cells after traumatic eye injury and induction of PVR. We demonstrated that upon infection with AAV carrying our construct, HEK293 cells and neurons in culture expressed the engineered HA-tagged PAS proteins. Their HA-tagged ectodomains were detected in the extracellular medium within minutes following stimulation with ionomycin and glutamate respectively. We used a rabbit PVR model of ocular trauma in which autologous blood was injected into the vitreous cavity of one eye after a surgical incision through the pars plana. Following the eye injury, we have isolated the eyeballs from experimental animals to evaluate the stage of PVR and the expression and activation of MPs after the ocular trauma.

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  • Anatomy and Physiology
  • Medicine and Medical Research

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